Shioura Krystyna M, Geenen David L, Goldspink Paul H
University of Illinois at Chicago, Department of Medicine/Section of Cardiology, 840 S. Wood St., M/C 715 Chicago, IL 60612, USA.
Am J Physiol Regul Integr Comp Physiol. 2008 Aug;295(2):R528-34. doi: 10.1152/ajpregu.90342.2008. Epub 2008 Jun 11.
Recent awareness of cardiovascular diseases as a number one killer of the middle-aged women has prompted interest in sex differences leading to heart failure (HF). Therefore, we evaluated cardiac function in female and male mice following myocardial infarction (MI) using the Millar pressure-volume (P-V) conductance system in vivo, at time points corresponding to early (2 wk), late compensatory hypertrophy (4 wk), and decompensation (10 wk) to HF. A significant deterioration of the load dependent and independent hemodynamic measurements occurred in both female and male mice during the early phase of hypertrophy. Later, compensatory hypertrophy was marked by a normalization of volumes to control levels in females compared with males. The most notable differences between sexes occurred in the measurements of cardiac contractility during the decompensation to HF. In females, there was a significant improvement in contractility compared with males, which was apparent in the load-independent measurements of preload recruitable stroke work (10 wk post-MI, female=48.7+/-8.0 vs. male=25.2+/-1.8 mmHg, P<0.05) and maximum dP/dt vs. maximum end-diastolic volume (10 wk post-MI, female=359+/-58 vs. male=149+/-28 mmHg.s(-1).microl(-1), P<0.05). Despite these differences, there were no differences in the heart weight to body weight ratio and infarct size between the sexes. These data demonstrate that compensatory hypertrophy is associated with an improvement in contractility and a delayed decompensation to HF in females. However, compensatory hypertrophy in males appears to be undermined by a steady decline in contractility associated with decompensation to HF.
近期，心血管疾病被视为中年女性的头号杀手，这引发了人们对导致心力衰竭（HF）的性别差异的关注。因此，我们使用Millar压力-容积（P-V）电导系统在体内评估了雌性和雄性小鼠心肌梗死（MI）后的心脏功能，时间点分别对应于心力衰竭早期（2周）、晚期代偿性肥大（4周）和失代偿期（10周）。在肥大早期，雌性和雄性小鼠的负荷依赖性和非依赖性血流动力学测量均出现显著恶化。随后，与雄性相比，雌性的代偿性肥大表现为容积恢复至对照水平。在心力衰竭失代偿期，两性之间最显著的差异出现在心脏收缩力的测量中。与雄性相比，雌性的收缩力有显著改善，这在非负荷依赖性的可招募前负荷搏功测量中很明显（心肌梗死后10周，雌性=48.7±8.0 vs. 雄性=25.2±1.8 mmHg，P<0.05），以及最大dP/dt与最大舒张末期容积的关系中（心肌梗死后10周，雌性=359±58 vs. 雄性=149±28 mmHg·s⁻¹·μl⁻¹，P<0.05）。尽管存在这些差异，但两性之间的心重与体重比和梗死面积并无差异。这些数据表明，代偿性肥大与雌性收缩力的改善以及心力衰竭失代偿的延迟有关。然而，雄性的代偿性肥大似乎因与心力衰竭失代偿相关的收缩力持续下降而受到影响。
